Jhanwar-Uniyal Meena, Albert Ladislau, McKenna Elise, Karsy Michael, Rajdev Priya, Braun Alex, Murali Raj
Department of Neurosurgery, New York Medical College, Valhalla, NY 10595, USA.
Adv Enzyme Regul. 2011;51(1):164-70. doi: 10.1016/j.advenzreg.2010.09.017. Epub 2010 Oct 28.
These findings emphasize that the mTOR pathway may contribute to maintenance of quiescence of CSCs, and provide a basis for manipulating CSCs in the treatment of GBM. Future research should focus on further defining the PI3K/Akt/mTOR molecular network in the regulation of stem cell quiescence and provide rationale for targeting the cancer-initiating cells of GBM.
这些发现强调，mTOR信号通路可能有助于维持癌症干细胞的静止状态，并为在胶质母细胞瘤治疗中操控癌症干细胞提供了依据。未来的研究应集中于进一步明确PI3K/Akt/mTOR分子网络在干细胞静止状态调控中的作用，并为靶向胶质母细胞瘤的癌症起始细胞提供理论依据。
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